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Fig. 8 | Cell Communication and Signaling

Fig. 8

From: Cholecystokinin type B receptor-mediated inhibition of A-type K+ channels enhances sensory neuronal excitability through the phosphatidylinositol 3-kinase and c-Src-dependent JNK pathway

Fig. 8

Schematic shows the regulation of CCK-BR on IA and the involvement of CCK-8/CCK-BR in pain sensitivity. CCK-8 stimulates the Go-protein coupled CCK-BR and thereafter releases the βγ subunits (Gβγ). The released Gβγ subsequently activates PI3K, which decreases the IA and induces neuronal hyperexcitability and pain hypersensitivity. PI3K catalyzes the conversion of PtdIns(4,5)P2 (PIP2) to PtdIns(3,4,5)P3 (PIP3), which serves as a second messenger that helps to activate Akt. However, neither PKA/PKC/Akt nor the direct binding of Gβγ with A-type channels contributes to the CCK-BR-mediated IA response. In mouse DRG neurons, PI3K signaling may activate Src, which then phosphorylates JNK to modulate IA. Whether the activated p-JNK would phosphorylates Kv channels encoding IA or in turn stimulated intermediate molecules still needs further examined

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Cell Communication and Signaling

ISSN: 1478-811X